糖尿病英文课件

DiabetesMellitus2025/2/281BeijingXuanwuHospitalDiabetesMellitusdefinitiontypessymptomsdiagnosisLaboratoryfindingstreatmentcomplications2025/2/282BeijingXuanwuHospitalDefinition-WHO(4/2000)Thetermdiabetesmellitusdescribesametabolicdisorderofmultipleaetiologycharacterizedbychronichyperglycaemiawithdisturbancesofcarbohydrate,fatandproteinmetabolismresultingfromdefectsininsulinsecretion,insulinaction,orboth2025/2/283BeijingXuanwuHospitalDefinitionAmetabolicconditioncharacterisedbyhighplasmaglucoselevelsandchronicvascularcomplicationsAvasculardiseaseaffectingsmallandlargearterieswithcoexistentmetabolicdisturbanceparticularlyhighplasmaglucoselevels2025/2/284BeijingXuanwuHospitalDiabetesMellitusdefinitiontypessymptomsdiagnosisLaboratoryfindingstreatmentcomplications2025/2/285BeijingXuanwuHospitalAetiologicalClassificationofDisordersofGlycaemiaType1

(beta–celldestruction,usuallyleadingtoabsoluteinsulindeficiency):Autoimmune:IdiopathicType2

(mayrangefrompredominantlyinsulinresistancewithrelativeinsulindeficiencytoapredominantlysecretorydefectwithorwithoutinsulinresistance)Otherspecifictypes

Geneticdefectsofbeta–cellfunction GeneticdefectsininsulinactionDiseasesoftheexocrinepancreasEndocrinopathies Drug–orchemical–inducedInfections Uncommonformsofimmune–mediateddiabetes OthergeneticsyndromessometimesassociatedwithdiabetesGestationaldiabetes2025/2/286BeijingXuanwuHospitalType1diabetesPreviouslyknownasIDDM(Insulindependentdiabetes)Ketosisprone:Usuallydiagnosedinyoungeragegroup(<30years)(Peakincidence11-13yr)Prevalencehighlyvariablebutapproximately0.20%withanincidenceof15-20per100000populationagedlessthan21Seasonalvariation-withlowestrateinspringandsummer2025/2/287BeijingXuanwuHospitalType1diabetesmellitusImmune-mediatedtype1diabetesacuteLADAlatentautoimmunediabetesinadults

Idiopathictype1diabetesmellitus2025/2/288BeijingXuanwuHospitalType1diabetesmellitusGeneticsEnvironmentalfactorVirusesChemicalagentsAutoimmune

Auto-antibodies:isletcellcytoplasmantibody(ICCA)isletcellsurfaceantibody(ICSA)glutamicaciddecarboxylaseantibodyGADA(64KD)Insulinantibody(IAA)

2025/2/289BeijingXuanwuHospitalType1diabetesThispresentationistheendpointofrecentandcontinuingbetacellfunctionresultinginneartotallossofInsulinproductionHyperglycaemiaitselfbegetsfurtherbetacelldestructionastreatmentwithinsulinoftenresultsina“honeymoon〞periodwhenthepatientcanoftenmanagewithoutinsulin2025/2/2810BeijingXuanwuHospitalType1diabetesmellitususuallyautoimmunedestructionof

insulin-producingpancreaticisletcells

overmonthsabsoluteinsulindeficiencyrapidpresentationwith

thirst,polyuria,weightloss,blurredvision

thrush,lethargy,dizziness.nausea,vomiting,abdominalcramps,andsuperficialinfectionusuallythinandketoticatpresentationAuto-antibodiesidentified:antiisletcell(ICCA.ICSA),antiGAD(64KD),antiInsulin(IAA)2025/2/2811BeijingXuanwuHospitalAprogressivemetabolicdisorder

characterisedby:

InsulinresistanceType2diabetes

-celldysfunction2025/2/2812BeijingXuanwuHospitalType2diabetesPreviouslyknownasNIDDMNonketosisprone:,diagnosis>30years1in1000populationasnewcaseseachyearInsidiouspresentationwithsymptomsofpolyuria,polydipsia,lethargy,weightloss,nausea,vomiting,abdominalcramps,blurredvisionandsuperficialinfection.OftendiscoveredatroutinemedicalThispresentationistheendpointofthegraduallossofbetacellfunctioninthesettingofInsulinresistanceStrong(90-100%)concordanceinTwinsReavan’ssyndromeorSyndromeX Insulinresistance2025/2/2813BeijingXuanwuHospitalType2diabetesUnderlyinginsulinresistancegeneticandethnicityObesityBMIWHRinactivity/lowphysicalfitnessintrauterine&childhoodfactorssmoking&drugsImpairedinsulinsecretionInsulinsecretionworsenswithtimepost-receptor

cellularmechanismsmechanism

unclearb-cell

exhaustion2025/2/2814BeijingXuanwuHospitalType2diabetesPrandialglucoseFastingglucoseInsulinresistanceInsulinsecretionPlasmaglucoseß-cell126mg/dLyears2025/2/2815BeijingXuanwuHospitalPancreatic

-cell

InsulinresistanceLiverHYPERGLYCAEMIAIslet

-celldegranulation

ReducedinsulincontentMuscle(PKC

Adiposetissue

Decreasedglucosetransport

&activity(expression)ofGLUT-4IncreasedlipolysisElevatedplasmaNEFA+-LowplasmainsulinIncreasedglucoseoutputElevatedTNF

Insulinresistanceand

-celldysfunctionproducehyperglycaemiaintype2diabetes2025/2/2816BeijingXuanwuHospitalTissueResponsestoInsulin

ResistanceorFailure

LIVERa.increasedglycogenhydrolysistoglucoseb.increasedgluconeogenesis.c.increasedtriacylglycerolhydrolysisandconversionofglyceroltoglucosed.increasedconversionofFAandproteintoketones(AcAcandBHB)e.increasedproteinandaminoacidcatabolismf.increasedproductionofurea2025/2/2817BeijingXuanwuHospitalMUSCLE

a.serumglucoseispoorlytakenupbymuscle(decreaseGLUTactivity)b.saturationofhexokinaseactivity,inabilitytoretaincellulargluasglu-6-PO4c.increasedLPLactivityandincreasedFAproductiond.increasedb-oxidation,butTCAisoverwhelmedbecauseATPishighalreadyee.increasedbreakdownofmuscleandserumproteinintoaminoacidsf.increasedtransferofNontoALA/GLNandsentbacktoliver2025/2/2818BeijingXuanwuHospitalADIPOSEa.increasedLPLandHSLsendmorefreeFAintobloodstreamb.glucosecannotbetakenintocellviaGLUT4forglycogensynthesisc.activeHSLmeansTAGsarenotbeingmadeandstored2025/2/2819BeijingXuanwuHospitalInsulinresistanceandinsulin

hypersecretionprecedetype2diabetesInsulinInsulinMacrovascularsensitivitysecretiondisease30%50%50%50%70–100%40%70%150%10%100%100%Type2diabetesIGTImpairedglucosemetabolismNormalglucosemetabolism2025/2/2820BeijingXuanwuHospitalClinicalReavansSyndromeInsulinresistanceHypertensionDyslipidaemia(increaseLDL,decreasedHDL)ObesityOtherfactors:hyperfibrinogenemia,hyperuricaemia,propensitytomicrovasculardiseases“Metabolicsyndrome〞inmostcasesoftype2diabetes2025/2/2821BeijingXuanwuHospitalabdominalobesityhighbloodpressureHDLcholesterol

VLDLtriglyceride

smalldenseLDL

hyperinsulinaemiaglucoseintolerancediabeteshyperuricaemiaPAI-1

fibrinogen

factorVII

microalbuminuriainsulinresistanceSyndromeofinsulinresistanceAKA Reaven’ssyndrome,syndromeX metabolicsyndrome2025/2/2822BeijingXuanwuHospitalType1diabetestypicalonset<30yearscanstartatanyagesuddenonsetseveresymptomsrecentweightlossusuallythinspontaneousketosisabsentC-peptidemarkersofautoimmunityType2diabetestypicalonset>20yearscanstartatanyagegradualonsetmaybenosymptomsoftennoweightlossusuallyobesenotketoticdetectableC-peptidenoautoimmunemarkers2025/2/2823BeijingXuanwuHospitalDiabetesinpregnancyco-existentornewlydiagnosedlifelongdiabetestype1type2(especiallyinSouthAsianwomen)otherspecifictypesofdiabetesgestationaldiabetes2025/2/2824BeijingXuanwuHospitalOthertypesofDiabetesGeneticdefectsofbeta–cellfunctionChr’me20,HNF4_(MODY1)Chr’me7,glucokinase(MODY2)Chr’me12,HNF1_(MODY3)Chr’me13,IPF–1(MODY4)MitochondrialDNA3243mutationGeneticdefectsininsulinactionTypeAinsulinresistanceLeprechaunismRabson–MendenhallsyndromeLipoatrophicdiabetes&OthersDiseasesoftheexocrine-pancreasFibrocalculouspancreatopathyPancreatitisTrauma/pancreatectomyNeoplasiaCysticfibrosisHaemochromatosis&OthersEndocrinopathiesCushing’ssyndromeAcromegalyPhaeochromocytomaGlucagonomaHyperthyroidismSomatostatinoma&Others

2025/2/2825BeijingXuanwuHospitalTypes-continuedInfectionsCongenitalrubellaCytomegalovirusOthers

Uncommonformsofimmune–mediateddiabetesInsulinautoimmunesyndrome(antibodiestoinsulin)Anti–insulinreceptorantibodies“StiffMan〞syndromeOthersDrug–orChemical–inducedDiabetes

NicotinicacidGlucocorticoidsThyroidhormoneAlpha–adrenergicagonistsBeta–adrenergicagonistsThiazidesDilantinPentamidineVacorInterferon–alphatherapyOthers2025/2/2826BeijingXuanwuHospitalPathophysiologyBecauseglucoseisnotgettingintocells,metabolismchangesCatabolismoffatsandproteinsinsteadofcarbohydratesLeadstoincreasedfattyacidsandketoacidsKetoacidosisresultsinloweringofpHDiabeticcomaDecompensatedmetabolicacidosisanddeath2025/2/2827BeijingXuanwuHospitalDiabetesMellitusdefinitiontypessymptoms

diagnosisLaboratoryfindingstreatmentcomplications2025/2/2828BeijingXuanwuHospitalSymptomsofdiabetesduetohyperglycaemiaHyperglycemiaDehydrationExcessivethirstandurinationExcessivehungerGlycosuria(gluspillsintourine:>180mg/dl)2025/2/2829BeijingXuanwuHospitalSymptomsofdiabetesduetohyperglycaemiaplasmaglucose

>renalthresholdabout12mmol/Lglucoseinurine

osmoticdiuresisurinevolumethirstgenitalthrushweightlosshyperglycaemiatiredness2025/2/2830BeijingXuanwuHospitalSymptomsofdiabetesduetohyperglycaemiahyperglycaemiaswellingoflens blurredvisioncerebraleffects lightheadedness malaise mentalchanges2025/2/2831BeijingXuanwuHospitalDiabetesMellitusdefinitiontypessymptomsdiagnosisLaboratoryfindingstreatmentcomplications2025/2/2832BeijingXuanwuHospitalADAdiagnosticcriteria(1997)Symptomsofdiabetes&acasualglucoseconcentrationmorethanorequalto200mg/dl(11.1mmol/l);Casualisdefinedasanytimeofdaywithoutregardstotimesincelastmeal.Theclassicsymptomsofdiabetesincludepolyuria,polydipsiaandunexplainedweightloss orFPGmorethanorequalto126mg/dl(7.0mmol/l).Fastingisdefinedasnocaloricintakeforatleast8hours or2hourPGmorethanorequalto200mg/dl(11.1mmol/l)duringanOGTT.ThetestshouldbeperformedasdescribedbyWHO,usingaglucoseloadcontainingtheequivalentof75gglucosedissolvedinwater2025/2/2833BeijingXuanwuHospitalWHOdiagnosticcriteria

wholeblood plasmaDiabetesmellitus

(fasting) >6.1mmol/l >7.0mmol/l2hourpostglucoseload >10.0mmol/l >11.1mmol/lIGT

(fasting) <6.1mmol/l <7.0mmol/l & &2hrpostglucoseload >6.7mmol/l >7.8mmol/lIFG

(fasting) >5.6mmol/l >6.1mmol/l &<6.1mmol/l &<7.0mmol/l2hrpostglucoseload ><6.7mmol/l <7.8mmol/lIGHimpairedglucosehomeostasis2025/2/2834BeijingXuanwuHospitalChangesfromOldcriteriaTheclass“ImpairedGlucoseTolerance〞isnowclassifiedasastageofimpairedglucoseregulation,sinceitcanbeobservedinanyhyperglycaemicdisorder,andisitselfnotdiabetes.ClinicalstageofImpairedFastingGlycaemiahasbeenintroducedtoclassifyindividualswhohavefastingglucosevaluesabovethenormalrange,butbelowthosediagnosticofdiabetes.GestationalDiabetesisretainedbutnowencompassesthegroupsformerlyclassifiedasGestationalImpairedGlucoseTolerance(GIGT)andGestationalDiabetesMellitus(GDM).2025/2/2835BeijingXuanwuHospitalDiagnosisofdiabetessymptoms+elevatedbloodglucoselevelORelevatedbloodglucoselevelsontwooccasions2025/2/2836BeijingXuanwuHospitalDifferentialDiagnosisHyperglycemiasecondarytoothercausesNondiabeticglycosuria2025/2/2837BeijingXuanwuHospitalDiabetesMellitusdefinitiontypessymptomsdiagnosisLaboratoryfindingstreatmentcomplications2025/2/2838BeijingXuanwuHospitalFPG:FastingPlasmaGlucoseCPG:CasualPlasmaGlucose(non-fasting)OGTT:OralGlucoseToleranceTest(75g)HemoglobinA1c(glycatedhemoglobin,glycosylatedhemoglobin)IndicatesaverageBGlevelsoverapprox.3months.%oftotalHgbattachedtoglucoseNormal:4-6%(DM:>8%)2025/2/2839BeijingXuanwuHospitalLaboratoryfindings

Glucose:FBG,2hrOGTT,FBGissimple,accurate,convenientforpatientGlycohemoglobinCreatinineUrinalysisglucoseketonebodiesMicroalbuminDyslipidemiaInsulinc-peptide2025/2/2840BeijingXuanwuHospitalDiabetesMellitusdefinitiontypessymptomsdiagnosisLaboratoryfindingstreatmentcomplications2025/2/2841BeijingXuanwuHospitalTreatmentofDiabetesNonPharmacologicalExerciseandEducationDiet,Lowinfat,lowrefinedsugars,highcarbohydrate,highfibre,lowcaloriesifobese,spacingofmeals(Healthyeating)LowcholesterolandtriglyceridedietifhyperlipidemiaAllType1patientswillrequireInsulinandtype2canbeondietonly,tabletsorinsulintreated2025/2/2842BeijingXuanwuHospitalTreatmentofdiabetestype1type2GDMdiet,exercise&insulindiet,exercisemetforminorsulphonylureaalonemetforminandsulphonylureametformin,sulphonylurea&thiazolidinedioneinsulindietinsulin2025/2/2843BeijingXuanwuHospitalDrugstotreathyperglycaemiaInsulinandinsulinanaloguesInsulinsecretagoguessulphonylureanon-sulphonylureaInsulinsensitizersbiguanidethiazolidinedioneIntestinalabsorptioninhibitorsacarboseorlistatlisproinsulinaspartinsulininsulinglarginegliclazide,glibenclamiderepaglinide,nateglinidemetforminrosiglitazone,pioglitazone2025/2/2844BeijingXuanwuHospitalsulphonylureaagentsgliclazide,glibenclamide,glimepiridebindtoreceptorsonisletcellsincreaseinsulinsecretionfromisletcellslongdurationofaction12-48hours

AdverseffectincreaseweightcancausehypoglycaemiacancauserashesContraindicationssulfaallergytype1DM,DKA2025/2/2845BeijingXuanwuHospitalMeglitinides

Mechanism:Bindstositeonbeta-cellmembraneleadingtoinsulinreleaseRapidoralabsorptionandeliminationforuseincontrollingpost-prandialhyperglycemia.Examples:repaglinide,nateglinideContraindicationsType1DM,DKAAdverseeffects:Hypoglycemia,weightgain2025/2/2846BeijingXuanwuHospitalmetforminlowersliverglucoseoutputincreasestissueglucoseuptakeactslikeaninsulinsensitizermildinductionofnauseapossibleinterferencewithfoodabsorptionnoeffectonweightusedalonedoesnotcausehypoglycaemiareducesriskofmyocardialinfarction1/3patientsgetdiarrhoea,windorabdominalpainnotusedinrenalfailure,heartfailureorsevereintercurrentillness2025/2/2847BeijingXuanwuHospitalMetforminToxicityRenallyexcreted,notmetabolizedPotentiallyfatallacticacidosisContraindications:renalinsufficiency(decreasesdrugclearance)hepaticdysfunction(decreaseslactatemetabolism)tissueanoxia(increaselactateproduction)2025/2/2848BeijingXuanwuHospitalacarbose-glucosidaseinhibitorblocksdigestionandabsorptionofsugarsfrombowellowersbloodglucoseandinsulinlevelsaftermealsweakantidiabeticdrugnoeffectonweightusedalonedoesnotcausehypoglycaemianotabsorbedintobody1/2patientsgetdiarrhoea,windorabdominalpain2025/2/2849BeijingXuanwuHospitala-glucosidaseinhibitortoxicityUnabsorbedCHO’s:Bacterialfermentationincolonresultsinabdominalpain,flatulencefromgasOsmoticdiarrheaElevatedserumtransaminasesMetabolizedandexcretedintheGItractSomemetaboliteisabsorbedinGIandrenallyexcretedContraindicatedforpatient’swithchronicorinflammatoryboweldiseaseRelativelyweakantidiabeticeffect,usuallyusedadjunctively.2025/2/2850BeijingXuanwuHospitalthiazolidinedioneagents

rosiglitazone,pioglitazone

Mechanism—BindtoPPAR-gammareceptorinperipheraltissuesmainlyskeletalmuscleResultinexpressionofcell-surfaceglucosetransporters.CautionsNotrecommendedinNYHAClassIII/IVCHFMaycausefluidretentionandprecipitateCHFMaycausemildanemia(?Dilutionaleffect)2025/2/2851BeijingXuanwuHospitalthiazolidinedioneagentsAssociatedwithweightgainLivertoxicityseeninolderTZD(troglitazone)butnotwithneweragents;recommendedtocheckLFTsq2mofor1styearofuse.AdvantagesNohypoglycemiaPossibleimprovementinvascularfunction2025/2/2852BeijingXuanwuHospitalThiazolidinedionetoxicityMetabolism:hepaticconjugationbytheCYP450systemExcretion:biliaryHepatotoxic,especiallytroglitazone,andcontraindicatedincasesofhepaticdysfunctionCancauseedemaandhypoglycemiawhenusedincombinationwithotherhypoglycemics2025/2/2853BeijingXuanwuHospitalTreatinghyperglycaemiaintype2diabetesdietarychangeexerciseobese

metforminnotobese

sulphonylureametformin&sulphonylureaglitazone&metforminOR

glitazone&sulphonylureainsulin±metforminAim:HbA1c<6.5%

Fastingglucose<7mmol/l2025/2/2854BeijingXuanwuHospitalinsulinanditsanaloguestheonlytreatmentfortype1diabetesalsousedfortype2diabetesandGDMcancausehypoglycaemiacausesweightgaincancausefluidretention2025/2/2855BeijingXuanwuHospitalThreemainprofiles:humanbio-engineered,porkorBovine.Variousregimens:twicedailysolubleandisophane,thricedailysoluble(pre-meal)andeveningisophane,rarelyoncedaily2025/2/2856BeijingXuanwuHospital2025/2/2857BeijingXuanwuHospitalBasal

bolusIntermediateNormalLong30:70mix2025/2/2858BeijingXuanwuHospitalRecommendedTreatment1stline:Dietandexercise2ndlineoralhypoglycemicmonotherapy(glyburide)adjunctiveto1stlinetreatmentSecond,third,andevenafourthclassofhypoglycemicscanactsynergisticallyformorediresituationsWhenallelsefails,backtotheneedle-insulintherapy2025/2/2859BeijingXuanwuHospitalEarlyAMHyperglycemia—PossibleCausesDawnphenomenonRiseinBGinearlymorningastheresultofpulsatilereleaseofinsulincounter-regulatoryhormones(growthhormoneandcortisol)SomogyiphenomenonPeriodofmorninghyperglycemiafollowingnocturnalhypoglycemia.Studieshavefailedtoshowthatthisoccurscommonly.NPHinsulingivenatdinnerwithwaningeffectbyAMLatenightsnacking2025/2/2860BeijingXuanwuHospitalDiabetesMellitusdefinitiontypesPrevalencesymptomsdiagnosistreatmentcomplications2025/2/2861BeijingXuanwuHospitalDiabeticComplicationsAcuteComplication:

hypoglycaemia,ketoacidosisoftenwithcoma(DKA), Hyperosmolarstateoftenwithcoma(HONK)Microvascularcomplications

Diabeticretinopathy,nephropathyandneuropathyMacrovascularcomplication

cerebrovascularaccidents,coronaryarterydisease,hypertension,peripheralvasculardiseasePregnancywithincreasedmaternalandfoetalmorbidity2025/2/2862BeijingXuanwuHospitalVascularcomplicationsofdiabetesretinopathynephropathyneuropathycoronaryarterydiseasecerebrovasculardiseaseperipheralvasculardisease2025/2/2863BeijingXuanwuHospitalDiabeticretinopathyleadingcauseofblindness95%ofdiabeticsubjectsshowsome

by15yearsafteronsetriskfactors:

age

diabetesduration

highbloodglucoselevels

highbloodpressure

geneticsmayprogressrapidlyduringpregnancy2025/2/2864BeijingXuanwuHospitalDiabeticretinopathyCataractformation(glycationα-crystallin)RetinopathyNonproliferative>microaneurysms>edemaProliferative(VEGF)>Newbloodvesselsthatextendintovitreous,bleeding>lossofvisionGlaucoma,intraocularpressure>oculartissuedamage2025/2/2865BeijingXuanwuHospitalNon-proliferativediabeticretinopathy(NPDR)EarlieststageMicroaneurismsandintraretinal“dotandblot〞hemorrhagesMacularedemaorhardexudatesat/nearmaculacancausevisualimpairmentProliferativediabeticretinopathy(PDR)Nonperfusionofretinaangiogenesisgrowthofabnormalnewvesselsextendingontoinnersurfaceofretinaorintovitreouscavity.Substantialriskforrupturehemorrhageorretinaldetachment.Treatedwithpanretinalphotcoagulation.2025/2/2866BeijingXuanwuHospitalDiabeticnephropathyAffects25%oftype1andtype2diabetespatientsRiskfactorssimilartothoseforretinopathyIsaprogressiveconditionleadingtorenalfailureCharacterisedbyproteinuriaandhighbloodpressure2025/2/2867BeijingXuanwuHospitalDiabeticnephropathyGlomerulosclerosis(Capillarybasementmembr.thickening)Microalbuminuria(30-300mg/24hr)Hyperfiltration(^GFR)Albuminuria(>300mg/24hr)HypertensionNephroticsyndrome(approx1/3ofType1progresstoendstagerenaldisrequiringdialysis)Renalfailure(

GFR,

Creat)2025/2/2868BeijingXuanwuHospitalDiabeticneuropathy

TypesofNeuropathySensoryPain/paresthesiasinfeetparticularlyatnightNumbnessin“stockingandglove〞distributionHighriskforfootulcerationAutonomicCardiovascular:restingtachycardia,painlessMI,orthostasisGI:esphagealdysfunction,gastroparesis,diabeticdiarrhea,constipation,fecalincontinenceGenitourinaryED,retrogradeejaculation,neurogenicbladderOther“gustatory〞sweating,heatintolerance2025/2/2869BeijingXuanwuHospitalDiabeticneuropathyAffectstype1andtype2diabetespatientssimilarlyRiskfactorssimilartothoseforretinopathymayleadtolossofsensationinfeetfootulcerationerectiledysfunctiongastroparesisandvomitingposturalhypotension2025/2/2870BeijingXuanwuHospitalMACROVASCULARCOMPLICATIONSMacrovascular(>70%hosp/deaths)60%ofpatientsdieofcoronarydisease10%ofpatientsdieofstroke10%sufferfromfatalcomplicationsrelatedtoperipheralvasculardisease2025/2/2871BeijingXuanwuHospitalCADAnginaMISilentinfarctCCFECGCardiacenzymesTroponinIExercisestresstestEchocardiographyAngiographyAngioplasty/CABG2025/2/2872BeijingXuanwuHospitalCVDTIAsCVAsDementiaCTscanCarotidDopplersTreatriskfactorsCarotidbypasssurgery2025/2/2873BeijingXuanwuHospitalPVDIntermittentClaudicationColdLegsPulselessLegFootUlcersGangreneDopplerStudiesDuplexScanningAngiographyAngioplastyTreatriskfactors2025/2/2874BeijingXuanwuHospitalDiabeticFootNeuropathyPVDCharcotArthropathyUlcerationMRIAngiography2025/2/2875BeijingXuanwuHospitalDiabeticKetoacidosisAcute(severaldaysratherthanhours)CausedbyInadequateinsulinInfectionStressUnderdosingFoodoralcoholbingeResultsinhyperglycemia&mobilizationoflipids2025/2/2876BeijingXuanwuHospitalDiabeticKetoacidosis(DKA)Type1Diabetics,SevereInsulinDef.Breakdownoffatstores>^FattyAcidsOxidation>KetoneBodies(^byglucagon)AccumulofAcetoaceticacid/βhydroxybutyricacid>^Plasma[H]>MetabolicKetoacidosis(Hydrationvsdehydration)2025/2/2877BeijingXuanwuHospitalDiabeticKetoacidosis(DKA)DKAresultsinalteredlipidmetabolismincreasedconcentrationsoftotallipids,cholesterol,triglycerides,andfreefattyacidsfreefattyacidsareshuntedintoketonebodyformationduetolackofinsulin;therateofformationexceedsthecapacityfortheirperipheralutilizationandrenalexcretionleadingtoaccumulationofketoacids,andthereforemetabolicacidosisWithprogressivedehydration,acidosis,hyperosmolality,anddiminishedcerebraloxygenutilization,consciousnessbecomesimpaired,andthepatientultimatelybecomescomatose2025/2/2878BeijingXuanwuHospitalClinicalManifestationsearlymanifestationsaremildandincludevomiting,polyuria,anddehydrationMoreseverecasesincludeKussmaulrespirations,odorofacetoneonthebreathabdominalpainorrigiditymaybepresentandmimicacuteappendicitisorpancreatitiscerebralobtundationandcomaultimatelyensue2025/2/2879BeijingXuanwuHospitalLaboratoryfindingsLaboratoryfindingsincludeglucosuria,ketonuria,hyperglycemia,ketonemia,andmetabolicacidosis.Serumamylasemaybeelevated.Leukocytosisiscommon2025/2/2880BeijingXuanwuHospitalDiagnosisDKAexistswhenthereishyperglycemia(>300mg/dL),ketonemia,acidosis,glucosuria,andketonuria2025/2/2881BeijingXuanwuHospitalDKAmustbedifferentiatedfromacidosisandcomaduetoothercauses:hypoglycemia,uremia,gastroenteritiswithmetabolicacidosis,lacticacidosis,salicylateintoxication,encephalitis2025/2/2882BeijingXuanwuHospitalTreatmentTreatmentisdividedinto3phasestreatmentofketoacidosistransitionperiodcontinuingphaseandguidanceGoalsoftreatmentofDKAintravascularvolumeexpansioncorrectionofdeficitsinfluids,electrolytes,andacid-basestatusinitiationofinsulintherapytocorrectcatabolism,acidosis2025/2/2883BeijingXuanwuHospitalKetoacidosisTreatmentAdministerinsulinRehydrateReplaceelectrolytesTreatacidosiswithbicarbonate2025/2/2884BeijingXuanwuHospitalIntravascularvolumeexpansiondehydrationismostcommonlyintheorderof10%initialhydratingfluidshouldbeisotonicsalinethisalonewilloftenslightlylowerthebloodglucoseTreatmentofelectrolyteabnormalitiesserumK+isoftenelevated,thoughtotalbodyK+isdepletedK+isstartedearlyasresolutionofacidosisandtheadministrationofinsulinwillcauseadecreaseinserumK+2025/2/2885BeijingXuanwuHospital“Maintenance〞IVfluidatarateof2000-2400cc/m2/dayconsistsof2/3NS(0.66%)orNSNSisaddedtoIVFwhenbloodglucoseis~250mg/dL5%Dextroseor5%GNSisaddedwhenbloodglucoseis~250mg/dL2025/2/2886BeijingXuanwuHospitalInsulinTherapycontinuousinfusionoflow-doseinsulinIV(~0.1U/kg/hr)iseffective,simple,andphysiologicallysoundgoalisto

slowlydecreaseserumglucose(<100mg/dL/hrfrequentlaboratoryandbloodgasanalysesareobtainedtoensureongoingresolutionofmetabolicacidosisInsulinisusedtotreatacidosis,nothyperglycemiainsulinshouldneverbestoppedifongoingacidosispersistsWhentheacidosisiscorrected,thecontinuousinsulininfusionmaybediscontinuedandsubcutaneousinsulininitiatedWiththeregimen,DKAusuallyisusuallyfullycorrectedin36to48hours2025/2/2887BeijingXuanwuHospitalsubclinicalcerebraledemaoccursinthemajorityofpatientstreatedwithfluidsandinsulinforDKACerebraledemaisthemajorlife-threateningcomplicationseeninthetreatmen